Identification of Jmjd1a as a STAT3 Downstream Gene in mES Cells

Ko, Song Yi; Kang, Hye Yoon; Lee, Hyun Sil; Han, Sang Yeul; Hong, Samin

doi:10.1247/csf.31.53

Cited by 18 publications

(8 citation statements)

References 35 publications

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“…+, Prdm1-GFP-positive cells; À, Prdm1-GFP-negative cells. Reduction or depletion of intracellular aKG during EpiLC differentiation conceivably curbs the activity of demethylating enzymes with key roles in preserving a naïve epigenetic state, such as the H3K9me2 demethylases KDM3A and KDM3B (Ko et al, 2006;Loh et al, 2007) and the TET family enzymes TET1 and TET2 (Costa et al, 2013;Hackett & Surani, 2014). H3 is used as a loading control.…”

Section: Discussionmentioning

confidence: 99%

Metabolic regulation of pluripotency and germ cell fate through α‐ketoglutarate

et al. 2018

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An intricate link is becoming apparent between metabolism and cellular identities. Here, we explore the basis for such a link in an in vitro model for early mouse embryonic development: from naïve pluripotency to the specification of primordial germ cells (PGCs). Using single‐cell RNA‐seq with statistical modelling and modulation of energy metabolism, we demonstrate a functional role for oxidative mitochondrial metabolism in naïve pluripotency. We link mitochondrial tricarboxylic acid cycle activity to IDH2‐mediated production of alpha‐ketoglutarate and through it, the activity of key epigenetic regulators. Accordingly, this metabolite has a role in the maintenance of naïve pluripotency as well as in PGC differentiation, likely through preserving a particular histone methylation status underlying the transient state of developmental competence for the PGC fate. We reveal a link between energy metabolism and epigenetic control of cell state transitions during a developmental trajectory towards germ cell specification, and establish a paradigm for stabilizing fleeting cellular states through metabolic modulation.

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Section: Discussionmentioning

confidence: 99%

Metabolic regulation of pluripotency and germ cell fate through α‐ketoglutarate

et al. 2018

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“…KDM3A (JMJD1A, JHDM2A) is a H3K9 demethylase that has been implicated in stem cell maintenance (Ko et al 2006; Loh et al 2007). KDM3A is overexpressed in renal carcinoma, presumably because it is the product of a HIF-responsive gene (Beyer et al 2008; Pollard et al 2008; Wellmann et al 2008; Sar et al 2009; Xia et al 2009; Krieg et al 2010).…”

Section: -Oxoglutarate-dependent Dioxygenases As Cancer Therapeutic mentioning

confidence: 99%

Cancer and Altered Metabolism: Potential Importance of Hypoxia-Inducible Factor and 2-Oxoglutarate-Dependent Dioxygenases

Wg¹

2011

Cold Spring Harbor Symposia on Quantitative Biology

144

134

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Otto Warburg noted decades ago that cancer cells maintain very high rates of glycolysis, converting glucose to lactate, despite sufficient oxygen to perform oxidative-phosphorylation, which is the more efficient means of generating energy (ATP) from glucose. This conundrum has generated considerable speculation as to whether altered metabolism, including altered glucose metabolism, is a cause or consequence of malignancy and, if the former, what benefits altered metabolism might confer upon cancer cells. Several lines of evidence, including the recent identification of mutations affecting Fumarate Hydratase, Succinate Dehydrogenase, and Isocitrate Dehydrogenase, have strengthened the notion that altered metabolism can cause cancer and a number of non-mutually exclusive models have been put forth to rationalize why cancer cells might benefit from a high rate of glycolysis and decreased oxidative phosphorylation. This chapter will focus on the role of HIF, 2-oxoglutarate, and 2-oxoglutarate-dependent enzymes in cancer and cancer metabolism.

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“…In murine ES cells, LIF-induced STAT3 activation plays an important role for self-renewal by influencing a variety of downstream target genes [74][75][76] or by interacting with several signaling pathways [77][78][79] and other molecules [80][81][82]. Although the central role of the LIF-STAT3 signaling has been well documented in murine ES cells, the function of this pathway has remained unclear in human ES cells (hESCs).…”

Section: Potential Role Of Stat3 In Regenerationmentioning

confidence: 99%

STAT3 and cardiac remodeling

et al. 2010

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Multiple in vitro and in vivo studies showed that the signal transducer and activator of transcription 3 (STAT3) protein is involved in cardiomyocyte protection and hypertrophy and via paracrine pathways impacts on the non-myocyte compartment, i.e., the vasculature and the extracellular matrix. In this regard, STAT3 interacts with a broad range of cellular and molecular mechanisms that direct remodeling processes in cardiac physiology (exercise, pregnancy) and pathophysiology (pressure overload, ischemia/reperfusion, myocardial infarction, and cardiotoxic agents). STAT3 is constitutively activated by a multitude of factors including cytokines, growth factors, neurohormones, mechanical load, and ischemia. It acts as a signaling molecule, a transcription factor and according to latest observations as a mitochondrial protein involved in energy production. In this review, we provide an overview on STAT3 signaling and summarize the current understanding of the role of STAT3 for different aspects of cardiac remodeling obtained from numerous experimental and clinical studies. Finally, we highlight and critically discuss STAT3 signaling as a possible target for future therapeutic approaches in the setting of cardiac remodeling.

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Identification of Jmjd1a as a STAT3 Downstream Gene in mES Cells

Cited by 18 publications

References 35 publications

Metabolic regulation of pluripotency and germ cell fate through α‐ketoglutarate

Metabolic regulation of pluripotency and germ cell fate through α‐ketoglutarate

Cancer and Altered Metabolism: Potential Importance of Hypoxia-Inducible Factor and 2-Oxoglutarate-Dependent Dioxygenases

STAT3 and cardiac remodeling

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